Abstract library

Introduction: Local tumor invasion represents the first step of the metastatic cascade of carcinomas, and requires changes in cell adhesion and migration properties of tumor cells. This biologic process is known as epithelial-mesenchymal transition (EMT). One key biochemical change associated with EMT is the loss of E-cadherin expression promoted by specific transcriptional repressors such as Snail, Slug, and Twist. Overexpression of EMT inducers increases other factors, such as FoxC2, although its role in EMT is poorly understood. Neuroendocrine tumors (NETs) of the gastroenteropancreatic (GEP) system, originated from the diffuse endocrine system, represent a heterogeneous group of tumors. Their prevalence has increased substantially over the past three decades, without substantial improvements in their clinical management, and their variable clinical course cannot be predicted by common clinicopathological parameters. Thus, new prognostic markers are urgently needed.

Introduction: Gastroenteropancreatic neuroendocrine tumors (GEP NETs) comprise a heterogeneous group of neoplasm with different histological patterns and biological behavior. Only limited information is available on immunohistochemical prognostic factors of disease. Alterations in the cell-cell adhesion system are closely associated with cell invasion and metastasis in many malignancies, including those of endocrine origin. Abnormal expression of E-cadherin and beta-catenin has been reported to play an important role in these processes. Caveolin-1 has recently been identified as a tumor metastasis modifier factor, which might increase the cell metastasis potential through the interaction with E-cadherin. However, the role of caveolin-1 in GEP NETs cell invasion remains unknown.

Introduction: Neuroendocrine tumors of the pancreas form an inhomogenous group of epithelial neoplasms. They differ from other types of pancreatic cancers by showing an extended survival of patients, which is due to a mostly slow proliferation rate of the tumor. However, some of these neuroendocrine tumors are characterized by an early onset of metastases, which cannot be predicted by any available method. The epithelial to mesenchymal transition (EMT) represents a central part of cell migration and metastasis. During EMT, cells loosen their cellular contacts, leave the tissue, and become migrating single cells. One of the integral compounds of cell adhesion represents the E-cadherin adhesion module, which contains mostly E-cadherin and several catenins. A loss of this adhesion module is associated with tumor progression, migration and metastasis in many types of cancer.

Introduction: E-cadherin plays a crucial role in the adhesion between epithelial cells and thus epithelial integrity. Moreover, germ line mutations in the E-cadherin gene (CDH1) causing loss of E-cadherin function (adhesion) leads to hereditary gastric cancer of the diffuse type, according to Laurén. Even sporadic gastric carcinomas of the diffuse type often lose E-cadherin expression due to mutations. Lack of E-cadherin has been recorded at an early phase in such carcinomas.

Introduction: Medullary thyroid carcinoma (MTC) is a rare tumor originating from thyroid parafollicular C cell. The only available treatment is surgical resection, which is not always feasible. Somatostatin and its receptors are expressed both in normal human thyroid C cells and in MTC, but their role has not been fully elucidated. The discovery of a truncated isoform of Sstr5, Sstr5TMD4, associated with increased invasiveness and aggressiveness in breast cancer, has opened new insight in the role of Sstr in cancers.

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